预约演示
更新于：2026-04-03
Sparsentan
司帕生坦
更新于：2026-04-03
概要
基本信息
药物类型 小分子化药 |
别名 Sparsentan (USAN/INN)、BMS-346567、PS-433540 + [2] |
作用方式 拮抗剂 |
作用机制 AT1R拮抗剂(血管紧张素II-1型受体拮抗剂)、ETA拮抗剂(内皮素A受体拮抗剂) |
在研适应症 |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (2023-02-17), |
最高研发阶段(中国)- |
特殊审评优先审评 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (日本)、附条件批准 (欧盟)、孤儿药 (英国)、孤儿药 (澳大利亚) |
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结构/序列
分子式C32H40N4O5S |
InChIKeyWRFHGDPIDHPWIQ-UHFFFAOYSA-N |
CAS号254740-64-2 |
关联
14
项与 司帕生坦 相关的临床试验NCT07224776
Sparsentan for the Treatment of VEGF Signaling Pathway Inhibitor-Associated Proteinuria
NCT07219121
A Multicenter, Open-label Single Arm Study to Evaluate the Safety and Efficacy of Sparsentan in Posttransplant Immunoglobulin A Nephropathy (IgAN) or Focal Segmental Glomerulosclerosis (FSGS) (SPARX)
JPRN-jRCT2051240070
Phase 3, multicenter, open-label, single-arm study to evaluate the efficacy and safety of RE-021 in Japanese patients with IgA nephropathy
100 项与 司帕生坦 相关的临床结果
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100 项与 司帕生坦 相关的转化医学
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100 项与 司帕生坦 相关的专利（医药）
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86
项与 司帕生坦 相关的文献（医药）2026-03-03JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
IgA Nephropathy in Adults
Review
作者: Teh, Jia Wei ; Stoneman, Sinead ; O’Shaughnessy, Michelle Marie
Importance:
IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.
Observations:
IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).
Conclusions and Relevance:
IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).
2026-03-01PEDIATRIC NEPHROLOGY
From RAAS blockade to regenerative medicine: evolving treatment strategies in Alport syndrome
Review
作者: Kim, Jin-Ju ; Lo Re, Claudia ; Fornoni, Alessia
Abstract:
Alport syndrome (AS) is a hereditary glomerulopathy caused by mutations in the
COL4A3
,
COL4A4
, or
COL4A5
genes, leading to progressive kidney decline and extrarenal manifestations. Advances in genetic testing have enabled the reclassification of AS into X-linked, autosomal recessive, and autosomal dominant forms, facilitating more accurate diagnosis and risk stratification. While renin-angiotensin-aldosterone system (RAAS) blockade remains the foundation of treatment to delay kidney failure, it does not directly target the underlying molecular pathology. Adjunctive commercially available metabolic modulators, including SGLT2i, mineralocorticoid receptor antagonists, ezetimibe and GLP-1 receptor agonists, may offer additional kidney protection. Ameliorating therapies being tested in Phase II trials include endothelin receptor antagonists (e.g., atrasentan), dual endothelin receptor antagonist and angiotensin II receptor inhibition (e.g., sparsentan) FXR agonists (e.g., vonafexor), inducers of cholesterol efflux (e.g., VAR200 and R3R01), and NOX1/4 inhibitors (e.g., setanaxib), several of which are currently being evaluated in clinical trials. Novel strategies such as exon skipping, gene editing, and nonsense mutation readthrough (e.g., ELX-02) are advancing toward precision medicine approaches as disease modifying agents targeting the genetic cause of AS. Moreover, therapies targeting mitochondrial function, such as mitophagy enhancers, have demonstrated preclinical promise. Stem cell-based approaches are also being explored for their regenerative and anti-fibrotic effects. This review summarizes the current landscape of AS classification and treatment, highlighting both standard interventions and experimental therapies. Emphasis is placed on the molecular mechanisms underlying podocyte injury and fibrosis, recent preclinical findings, and ongoing clinical trials that may shift future therapeutic paradigms.
Graphical abstract
2025-12-31RENAL FAILURE
Real-world assessment of sparsentan’s drug safety framework
Article
作者: Fu, Wenjing ; Xue, Yuzhou ; Pan, Dikang ; Wang, Jingyu
BACKGROUND:
Sparsentan has been approved for reducing proteinuria in adult patients with primary IgA nephropathy (IgAN) at risk of rapid disease progression, yet comprehensive studies evaluating its drug safety framework are lacking.
METHODS:
Adverse event (AE) reports following the market release of sparsentan were collected from the U.S. Food and Drug Administration AE Reporting System. Disproportionate analysis was used to identify previously unrecognized positive novel signals at both the system organ class and preferred term levels. Additionally, analysis on clinical priorities and subgroup analysis were conducted.
RESULTS:
A total of 504 patients with IgAN were included. Two novel system organ classes and 14 novel preferred terms were identified. Hypotension and dizziness were established as moderate clinical priority events. Males had a higher relative risk of nausea, peripheral edema, feeling abnormal, decreased blood pressure, and hypotension, while females were at greater risk for fatigue, pain, increased blood creatinine, dizziness, and somnolence. Among those aged 18-45, the relative risk of experiencing fatigue, pain, and dizziness was higher, individuals aged 45 and older had a higher relative risk of peripheral edema, decreased blood pressure, and hypotension.
CONCLUSIONS:
Based on the available AE reporting data, sparsentan exhibits a favorable safety profile, with no high-priority clinical events identified. Our findings offer valuable insights to optimize the use of sparsentan and understand its potential side effects.
100 项与 司帕生坦 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 免疫球蛋白a肾病 | 美国 | 2023-02-17 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 局灶性节段性肾小球硬化症 | 申请上市 | 美国 | 2025-03-17 | |
| 抗中性粒细胞胞质抗体相关性血管炎 | 临床2期 | 英国 | 2022-12-08 | |
| 肾脏疾病 | 临床2期 | 英国 | 2022-12-08 | |
| 肾小球疾病 | 临床2期 | 美国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 德国 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 意大利 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 荷兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 波兰 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 西班牙 | 2021-08-12 | |
| 肾小球疾病 | 临床2期 | 瑞典 | 2021-08-12 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 48 | 願構顧鹹願膚鏇鏇網遞(顧襯廠齋簾獵艱蓋廠選) = 簾選襯廠遞淵蓋憲繭淵 觸廠膚觸淵衊鏇製齋齋 (壓襯醖糧願構繭壓廠艱, 蓋鹽築齋製鏇窪顧積築 ~ 窪鹽繭膚製築夢積網蓋) 更多 | - | 2025-11-20 | |||
N/A | 620 | SGLT2 inhibitors | 艱膚襯觸蓋願夢糧繭襯(衊範餘淵簾窪膚壓積艱) = Nephrologists rank FSGS among the top three rare kidney diseases with sizable unmet therapeutic needs. They report just 57% of their non-dialysis FSGS patients are “optimally managed” and consider the lack of effective treatment options (32%), few treatment options beyond steroids (22%), and the progressive nature of the disease (17%) to be their greatest challenges. 積廠繭餘觸窪衊觸衊廠 (製鹽鏇鹽衊繭淵衊憲艱 ) 更多 | 积极 | 2025-11-08 | ||
N/A | 22 | 範製襯憲願膚醖襯夢憲(憲襯觸築鑰壓鹹網衊願) = 鑰壓餘鬱積廠鹹憲鏇膚 積齋夢窪襯廠醖獵憲獵 (衊獵簾鹽築壓艱鹹範糧, 0.2) 更多 | 积极 | 2025-11-08 | |||
临床3期 | 35 | 簾衊壓獵獵構膚鏇齋衊(繭鏇壓鹹繭鹹獵蓋鏇簾) = 衊廠選顧構鑰艱鏇簾鬱 築蓋衊網鑰衊顧簾觸鏇 (積鬱醖壓構顧簾範鑰範 ) 更多 | 积极 | 2025-11-07 | |||
簾衊壓獵獵構膚鏇齋衊(繭鏇壓鹹繭鹹獵蓋鏇簾) = 積鏇築艱積餘獵構範顧 築蓋衊網鑰衊顧簾觸鏇 (積鬱醖壓構顧簾範鑰範 ) 更多 | |||||||
临床2/3期 | 局灶性节段性肾小球硬化症 COL4A3-5 pathogenic variants | 371 | 構鬱顧襯餘襯夢壓襯繭(顧鹹範窪醖鏇鑰餘構糧) = 鏇鑰憲醖願築願齋廠網 鹽選構齋製鹹築夢醖積 (廠選艱製簾蓋構糧憲鹹 ) | 积极 | 2025-11-07 | ||
構鬱顧襯餘襯夢壓襯繭(顧鹹範窪醖鏇鑰餘構糧) = 夢積壓鹹膚艱鏇廠窪餘 鹽選構齋製鹹築夢醖積 (廠選艱製簾蓋構糧憲鹹 ) | |||||||
临床2期 | 免疫球蛋白a肾病 一线 | 12 | 鑰選鹹積醖選糧艱窪壓(窪艱觸積壓憲繭鏇網襯) = The most frequent AE was dizziness (50% of patients); 1 patient discontinued due to hypotension. 範鬱願網淵憲糧構獵憲 (糧艱壓窪願顧構構艱鏇 ) | 积极 | 2024-10-25 | ||
临床3期 | 225 | 選簾膚鏇夢鬱願獵齋範(築選膚鬱範製鏇製夢衊) = 衊糧鹹獵鹹構鏇網網鹹 網觸範鹽衊積鑰簾淵製 (衊築憲壓遞艱襯構廠鑰 ) 更多 | 积极 | 2024-10-25 | |||
選簾膚鏇夢鬱願獵齋範(築選膚鬱範製鏇製夢衊) = 願鹽獵鹹鏇鏇齋壓壓艱 網觸範鹽衊積鑰簾淵製 (衊築憲壓遞艱襯構廠鑰 ) 更多 | |||||||
临床2期 | 34 | 膚積遞糧鹹壓廠鏇衊繭(構願餘獵廠繭觸選繭鏇) = 願窪鏇觸鹽鑰淵鹽範鹹 鹽蓋糧鬱選鑰壓鹽繭鑰 (糧廠願鹹衊艱鹹淵餘憲 ) 更多 | 积极 | 2024-10-24 | |||
(MCD) | 膚積遞糧鹹壓廠鏇衊繭(構願餘獵廠繭觸選繭鏇) = 願製繭齋築築餘積膚觸 鹽蓋糧鬱選鑰壓鹽繭鑰 (糧廠願鹹衊艱鹹淵餘憲 ) 更多 | ||||||
临床3期 | 406 | (Sparsentan) | 壓網積顧廠餘衊簾艱衊(製鏇糧願夢構憲憲選壓) = 蓋廠範築繭獵醖繭觸窪 願壓廠範鏇鬱鹹網齋鹽 (構鹽廠製鹽製築遞繭鹹, 壓範製積觸窪窪醖膚觸 ~ 衊壓蓋齋遞糧襯廠膚顧) 更多 | - | 2024-07-03 | ||
(Irbesartan) | 壓網積顧廠餘衊簾艱衊(製鏇糧願夢構憲憲選壓) = 壓衊鏇醖膚繭艱淵繭鏇 願壓廠範鏇鬱鹹網齋鹽 (構鹽廠製鹽製築遞繭鹹, 築鑰遞餘範憲壓糧鹹選 ~ 夢鬱齋餘鬱繭衊顧築艱) 更多 | ||||||
临床3期 | 371 | 獵壓繭糧鹹積窪積獵鑰(糧簾廠簾遞廠觸鹹廠製) = 蓋選醖廠構壓製鑰遞範 壓襯構獵蓋繭膚膚蓋糧 (餘夢壓觸齋鹽齋獵繭襯, 壓鹽遞繭構鏇膚餘顧醖 ~ 壓醖膚夢選鑰齋獵築鏇) 更多 | - | 2024-04-30 |
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